Clinical Pathophysiology Of Cardiovascular Diseases

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Clinical Pathophysiology Of Cardiovascular
Diseases
Ph. D., M D. Svitlana Dzyha
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• Blood pressure is one of the most variable but
  best regulated functions of the body.
• The purpose of the control of blood pressure is
  to keep blood flow constant to vital organs such
  as the heart, brain, and kidneys.
• The continuous elevation of blood pressure that
  occurs with hypertension is a contributor to
  premature death and disability due to its effect
  on the heart, blood vessels, and kidneys.

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• The level of blood pressure in the healthy
  people is the very stable value.
• The stability of blood pressure is supported by
  regulative systems.
• Hayton (1974) divided them into two groups
  hemodynamic system and regulative system.

Arterial blood pressure normal range Systolic
100 - 125 (equilibration 100 - 139) mm
Hg Diastolic 70 - 80 (equilibration 60 - 89) mm
Hg
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Regulation of arterial pressure (?P)by
hemodynamic system
Formula ?P CO PR CO cardiac output PR
peripheral vascular resistance (depended to
arterioles tone)

• CO leads to PR and ?P
  normalizes finally

PR leads to CO and ?P normalizes
finally
AP normal range Systolic 100 - 125
(equilibration 100 - 139) mm Hg Diastolic 70 -
80 (equilibration 60 - 89) mm Hg
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Mechanisms of Blood Pressure Regulation

• Short-term regulation
• neural mechanisms
• hormonal mechanisms
• Long-term regulation

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NEURAL MECHANISMS
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• Location and innervation of the aortic arch and
  carotid sinus baroreceptors and the carotid body
  chemoreceptors.

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Regulative systems

• 1. Barroreceptors of aorta arch and sinus
  caroticus

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Regulative systems
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Role of the vasopressin in arterial hypertension
pathogenesis
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Classification
Arterial hypertension
AP above 139/89 mm Hg
Primary
Secondary

• Arterial hypotension

AP less than 100/60 mm Hg
Acute
Chronic
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Arterial hypertension (?H)

• AP elevation
• (value above 139/89 mm Hg), which is resulted
  from rising of peripheral vessels resistance
• (one of the most common cardiovascular disorders)

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Classification

• Primary AH
• (essential, hypertonic disease)

Secondary AH (that is happened in 10 - 20
cases). Its a symptom of some disease course
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Etiology (primary AH)
Reason is unknown. AH is polyetiological
disease. AH arises on the ground of genetically
peculiarities of metabolism. That is possible
to have genetically defect of the systems, which
control relaxation of the smooth muscle cells of
the arterioles.
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Contributing factors
Risk Factors

• Family history of hypertension

Race
Age-related increases in blood pressure
Diabetes mellitus
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Contributing factorsLifestyle Factors
High sodium intake
Stress
Physical inactivity
Excessive calorie intake and obesity
Excessive alcohol consumption
Oral contraceptive drugs
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Pathogenesis
AP ?O ? PR
Increase of circulative blood volume (CBV)

• Emotional excitement
• (SNS activation)

Cardiac output (C?) increase
Peripheral vessels resistance increase
Kidney functions violation
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Pathogenesis
Increase of circulative blood volume (CBV)
NaCl (intake more 5 g/day)
Reasons
Decrease Na excretion by kidney (kidney diseases)
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Pathogenesis
1. CBV increase
Na accumulation in vessels smooth muscle wall and
increase of its osmotic pressure
Na retention in blood
Blood osmotic pressure increase
Vessels wall edema
Vessels smooth muscle sensitivity to
vasoconstrictive influences increase
(noradrenalin, adrenalin, endothelin, angiotensin)
Hypervolemia
Vessels narrowing
Cardiac output increase
Vessels spasm
Peripheral vessels resistance increase
AP elevation
Formula ?P CO PR
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Pathogenesis
2. Cardiac output increase (CO)
Circulative blood volume increase (CBV)
Reasons
Emotional stress
Physical (overload) stress
Hyperthyroidism
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Pathogenesis
2. Cardiac output increase
SAS activation
Adrenalin excretion
Increase of cardiac contractility force
Increase of heart beats
Increase of cardiac output
AP elevation
Formula ?P CO PR
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Pathogenesis
3. SAS activation
SAS activation
Suprarenal glands activation
Interaction adrenalin and alpha-adrenoreceptors
Venues smooth muscles spasm
Arterioles smooth muscles spasm
Increase of circulative blood in big blood circle
?drenalin
Noradrenalin
adrenoreceptors of heart
alpha-adrenoreceptors of vessels
Arterioles narrowing
Increase of CBV
Arterioles narrowing
PR increase
CO increase
CO increase
AP increase
Formula ?P CO PR
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Pathogenesis
4. Kidney functions violation
Long time spasm of kidney arteries

• Angiotensin 2 effects
• Smooth muscles contraction in the vessels
• Stimulation of the vasoactive center in brain
• Noradrenalin excretion increase
• Adrenalin excretion increase from suprarenal
  glands
• Aldosteron excretion increase from suprarenal
  glands (Na retention due to kidney)

AP decrease in renal capillaries
Activation of JGA
Renin excretion
Angiotensin 2 synthesis
AP increase
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Depressive function of kidney synthesis of the
substances for AP reduce
dilates renal arteries, reduces renin synthesis
and reduces Na reabsorbing in kidney
PG ? 2
! ! ! Exhaustion of kidney depressive function
leads to arterial hypertension stabilization
Phospholipid Renin Inhibitor
Angiotensinase
Phosphatydilcholin alkali ethers
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Increase of vesseles resistance

• It is the defining mechanism. Irrespective of
  first reason, in the patients with hypertonic
  disease almost always increases peripheral
  resistance.
• It is considered, that the essence hypertonic
  disease just is in increase of peripheral
  vessels tonus. Hyperkinetic phase, which is
  connected to increase of cardiac output, happens
  only at early stages of disease and not in all
  patients.

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The hereditary predisposition
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Etiologysecondary ?H

• Renal
• (resulted from kidney pathology)

Acute renal failure
Glomerulonephritis
Pyelonephritis
Kidney damage at collagenosis
Acute urinary tract obstruction
Kidney amiloidosis
Kidney tumor
Diabetic nephropathy
Nephropathy of the pregnant
Hereditary defect of renal vessels
Renal vessels atherosclerosis, embolism or
thrombosis
Polycystic kidney disease
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Etiologysecondary ?H
4. Endocrinopathy (develops in the result of
endocrine glands pathology)
Acromegaly (Somatotropin over production by the
pituitary gland anterior part)
Hyperaldosteronism (aldosteron over excretion by
suprarenal glands)
Cushing's disease (Adrenocorticotropin over
production by the pituitary gland anterior part)
Menopause (age-depended decrease of female gonads
activity estrogens excretion decrease) Possible
mechanism deficit of NO synthesis by
endotheliocytes
Pheochromocytoma
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Etiologysecondary ?H
5. Neurogene (is accompanying to nerves system
pathology)
Encephalitis
Brain tumor
Brain trauma
Brain ischemia
Brain hemorrhage
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Etiologysecondary ?H
6. Cardiac
Heart failure
Heart defect
7. Drug-induced
Drugs, which cause vessels spasm (influent on
kidney), hormonal contraceptives
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Arterial hypertension after-effects
1st period functional violations (heart
hypertrophy)

• 2d period
• Pathological changes in arteries and arterioles
  (dystrophy)
• Arterioles sclerosis
• Arterioles wall infiltration by plasma (leads to
  dystrophy)
• Arterioles necrosis (hypertonic crisis arises in
  clinic)
• Veins wall thickening

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Arterial hypertension after-effects
3d period Secondary changes in organs and systems
CNS brain hypoxia neurons destruction
apoplexy (because vessels destruction and rupture
leads to brain hemorrhages and brain destruction)
Kidney (nephrosclerosis and chronic kidney
insufficiency)

• Organs of vision
• retinopathy (retinas vessels injury)
• hemorrhages and separation (exfoliation) of
  retina, that leads to blindness

Heart Decompensate heart failure
Endocrine system Glands atrophy and sclerosis